The L-type voltage-dependent Ca(2+) channel EGL-19 controls body wall muscle function in Caenorhabditis elegans

Caenorhabditis elegans is a powerful model system widely used to investigate the relationships between genes and complex behaviors like locomotion. However, physiological studies at the cellular level have been restricted by the difficulty to dissect this microscopic animal. Thus, little is known about the properties of body wall muscle cells used for locomotion. Using in situ patch clamp technique, we show that body wall muscle cells generate spontaneous spike potentials and develop graded action potentials in response to injection of positive current of increasing amplitude. In the presence of K(+) channel blockers, membrane depolarization elicited Ca(2+) currents inhibited by nifedipine and exhibiting Ca(2+)-dependent inactivation. Our results give evidence that the Ca(2+) channel involved belongs to the L-type class and corresponds to EGL-19, a putative Ca(2+) channel originally thought to be a member of this class on the basis of genomic data. Using Ca(2+) fluorescence imaging on patch-clamped muscle cells, we demonstrate that the Ca(2+) transients elicited by membrane depolarization are under the control of Ca(2+) entry through L-type Ca(2+) channels. In reduction of function egl-19 mutant muscle cells, Ca(2+) currents displayed slower activation kinetics and provided a significantly smaller Ca(2+) entry, whereas the threshold for Ca(2+) transients was shifted toward positive membrane potentials.